Magic™ Anti-NOS (Phospho Y151) polyclonal antibody

The enzyme nitric oxide synthase has been associated with suicide behavior. NOS1, NOS2 and NOS3 genes are implicated in the production of nitric oxide. However, the association between NOS genes and suicide behavior has not yet been established. To assess the association of Nitric Oxide Synthase (NOS) genes and suicide behavior we performed a systematic review a meta-analysis. We searched articles published in three electronic databases, PubMed, Scopus and Web of Sciences, up to February 2019. We used keywords and combinations NOS, NOS1, NOS2, NOS3 and suicide. Only articles that met the inclusion criteria were included. To assess the association between NOS genes and suicide behavior we used allelic, dominant and recessive models, as well as homozygous and heterozygous comparisons. The pooled results showed that rs2682826 of Nitric Oxide Synthase 1 gene (NOS1) increased the risk for suicide attempt in the allelic (OR: 1.34; 95 CI: 1.00-1.78), recessive (OR: 1.45; 95 CI:1.06-1.98) and heterozygous (OR: 1.41; 95 CI: 1.09-1.81) models. We found that the rs2682826 of NOS1 could increase the risk for suicide attempt. However, these results should only be taken as exploratory; more studies are necessary to determine the association between NOS genes and suicide behavior.

Orientia tsutsugamushi is the causative agent of scrub typhus. It is an obligate intracellular bacterium that grows only in eukaryotic cells. Macrophages play an important role in innate immunity by surveilling the human body for pathogens. In present study, it was demonstrated that O. tsutsugamushi propagated well in LPS-activated RAW 264.7 macrophages, but not in non-activated macrophages. In LPS-activated macrophages, the expression of Nos2, which encodes the inducible nitric oxide (NO) synthase (iNOS), was highly upregulated compared to those in non-activated macrophages. Parallel to this upregulation, high NO production was observed in LPS-activated macrophages. Transmissible electron microscopy showed that O. tsutsugamushi replicated in the cytosol of macrophages. Thus, O. tsutsugamushi was thought to escape the phagosomes at an early stage of phagosome maturation to avoid the bactericidal effect of NO. Furthermore, O. tsutsugamushi growth was enhanced in NO donor-supplied RAW 264.7 macrophages, as well as in LPS-activated, but not in non-activated macrophages. Consequently, these results suggested that NO was rather essential for enhancing the replication of O. tsutsugamushi in RAW 264.7 macrophages, despite the typically detrimental effects of NO against intracellular pathogens. In the present study, NO was suggested to activate specific pathways to enhance the growth of O. tsutsugamushi. (C) 2017 Elsevier Ltd. All rights reserved.